1. Field of Invention
This application relates to cerebral blood pressure autoregulation and more particularly to devices and methods to diagnose and/or treat cerebrovascular autoregulation in a patient.
2. Discussion of Related Art
The contents of all references, including articles, published patent applications and patents referred to anywhere in this specification are hereby incorporated by reference.
Cerebral pressure autoregulation is defined as the maintenance of a constant cerebral blood flow (CBF) in the face of changing cerebral perfusion pressure (CPP). In health, this process protects the brain during transient changes in the arterial blood pressure (ABP) from diminished or excessive blood flow. Traumatic brain injury (TBI) (Muizelaar J P, Marmarou A, DeSalles A A, et al. Cerebral blood flow and metabolism in severely head-injured children. part 1: Relationship with GCS score, outcome, ICP, and PVI. J Neurosurg. 1989; 71(1):63-71; Muizelaar J P, Ward J D, Marmarou A, Newlon P G, Wachi A. Cerebral blood flow and metabolism in severely head-injured children. part 2: Autoregulation. J Neurosurg. 1989; 71(1):72-76; Vavilala M S, Muangman S, Tontisirin N, et al. Impaired cerebral autoregulation and 6-month outcome in children with severe traumatic brain injury: Preliminary findings. Dev Neurosci. 2006; 28(4-5):348-353), stroke (Dawson S L, Panerai R B, Potter J F. Serial changes in static and dynamic cerebral autoregulation after acute ischaemic stroke. Cerebrovasc Dis. 2003; 16(1):69-75), meningitis (Berkowitz I D, Hayden W R, Traystman R J, Jones M D, Jr. Haemophilus influenzae type B impairment of pial vessel autoregulation in rats. Pediatr Res. 1993; 33(1):48-51; Slater A J, Berkowitz I D, Wilson D A, Traystman R J. Role of leukocytes in cerebral autoregulation and hyperemia in bacterial meningitis in rabbits. Am J Physiol. 1997; 273(1 Pt 2):H380-6), cardiopulmonary bypass, and deep hypothermic circulatory arrest (O'Rourke M M, Nork K M, Kurth C D. Neonatal cerebral oxygen regulation after hypothermic cardiopulmonary bypass and circulatory arrest. Crit Care Med. 2000; 28(1):157-162) are examples of insults that have been shown to impair pressure autoregulation and have large-scale clinical impact. An impairment of autoregulation narrows the range of blood pressures at which flow is matched to metabolic needs. Optimal management of CPP for limiting tissue hypoxia at low CPP or edema at high CPP in these patients is critical but difficult to achieve because of limited monitoring capabilities. Despite the recent surge of multimodal neuromonitoring, optimal ABP and CPP have not been defined.
It has been postulated that continuous monitoring of autoregulatory vasoreactivity allows detection of an “optimal CPP” and titration of blood pressure into a range that maximizes vasoreactivity to perturbations in CPP (Steiner L A, Czosnyka M, Piechnik S K, et al. Continuous monitoring of cerebrovascular pressure reactivity allows determination of optimal cerebral perfusion pressure in patients with traumatic brain injury. Crit Care Med. 2002; 30(4):733-738). Autoregulation is measured by quantifying the consequence of changing blood pressure on CBF or its surrogate, and the methods have been extensively reviewed (Panerai R B. Assessment of cerebral pressure autoregulation in humans—a review of measurement methods. Physiol Meas. 1998; 19(3):305-338). Changes in ABP can be induced via drugs, tilt-table, or thigh cuff (Aaslid R, Lindegaard K F, Sorteberg W, Nornes H. Cerebral autoregulation dynamics in humans. Stroke. 1989; 20(1):45-52), or they can occur spontaneously. Using spontaneous changes in ABP is preferable to inducing ABP changes in an unstable patient with an acute intracranial process. However, relying on spontaneous and often subtle ABP fluctuations for this measurement results in an inferior signal-to-noise ratio.
Diverse surrogates of CBF are suitable for continuous monitoring of autoregulation and include flow velocity, measured by transcranial Doppler (Czosnyka M, Smielewski P, Kirkpatrick P, Menon D K, Pickard J D. Monitoring of cerebral autoregulation in head-injured patients. Stroke. 1996; 27(10):1829-1834); red blood cell flux, measured by laser-Doppler (Lam J M, Hsiang J N, Poon W S. Monitoring of autoregulation using laser doppler flowmetry in patients with head injury. J Neurosurg. 1997; 86(3):438-445); parenchymal oxygen tension, measured using a Licox monitor (Lang E W, Czosnyka M, Mehdorn H M. Tissue oxygen reactivity and cerebral autoregulation after severe traumatic brain injury. Crit Care Med. 2003; 31(1):267-271; Jaeger M, Schuhmann M U, Soehle M, Meixensberger J. Continuous assessment of cerebrovascular autoregulation after traumatic brain injury using brain tissue oxygen pressure reactivity. Crit Care Med. 2006; 34(6):1783-1788); and cerebral tissue oxyhemoglobin saturation, measured by transcranial near-infrared spectroscopy (NIRS) (Tsuji M, Saul J P, du Plessis A, et al. Cerebral intravascular oxygenation correlates with mean arterial pressure in critically ill premature infants. Pediatrics. 2000; 106(4):625-632). Slow waves of intracranial pressure (ICP) reflecting vessel diameter changes in the autoregulatory process have also been correlated to ABP for an index describing autoregulation (Czosnyka M, Smielewski P, Kirkpatrick P, Laing R J, Menon D, Pickard J D. Continuous assessment of the cerebral vasomotor reactivity in head injury. Neurosurgery. 1997; 41(1):11-7; discussion 17-9). An ideal CBF surrogate for an index of autoregulation would be noninvasive and require minimal caregiver attention. It would provide a continuous signal with time resolution sufficiently fine to discriminate changes in frequencies relevant to autoregulation, and that signal would be a close proxy for CBF. There is thus a need for improved methods and devices for diagnosing cerebrovascular autoregulation in patients.